rituximab, Rituxan

Omudhome Ogbru, PharmD

Dr. Ogbru received his Doctorate in Pharmacy from the University of the Pacific School of Pharmacy in 1995. He completed a Pharmacy Practice Residency at the University of Arizona/University Medical Center in 1996. He was a Professor of Pharmacy Practice and a Regional Clerkship Coordinator for the University of the Pacific School of Pharmacy from 1996-99.

Jay W. Marks, MD

Jay W. Marks, MD, is a board-certified internist and gastroenterologist. He graduated from Yale University School of Medicine and trained in internal medicine and gastroenterology at UCLA/Cedars-Sinai Medical Center in Los Angeles.

GENERIC NAME: rituximab

BRAND NAME: Rituxan

DRUG CLASS AND MECHANISM: Rituximab is an intravenous drug that is
used to treat rheumatoid arthritis and
B-cell non-Hodgkin's lymphoma. It belongs
to a class of drugs called monoclonal antibodies. Other monoclonal antibodies
include trastuzumab (Herceptin) and gemtuzumab ozogamicin (Mylotarg). Tumor
cells (like most normal cells) have receptors on their surfaces. Many kinds of
chemicals, proteins, etc., on the outside of the cell can attach to these
receptors. When they do, they can cause changes to occur within the cells. One
receptor, present in more than 90% of B-cell non-Hodgkin's lymphomas, is called
CD20. Molecules that attach to CD20 can affect the growth and development of the
tumor cells and, sometimes, the production of new tumor cells. Rituximab is a
man-made antibody that was developed using cloning and recombinant DNA
technology from human and murine (mice or rat) genes. Rituximab is thought to
attach to the CD20 receptor and cause the tumor cells to disintegrate (lyse). In
some non-Hodgkin's lymphomas, it also prevents the production of more tumor
cells. Rituximab was approved by the FDA in 1997. In the treatment of rheumatoid arthritis, rituximab is used when other biologic medications (TNF-blockers, such
as infliximab,
[Remicade] etanercept
[Enbrel], or adalimumab
[Humira]) have failed to be effective. The
effectiveness of rituximab is a result of it temporarily depleting the number of
B-cells, cells of the immune system that are important in promoting inflammation
in rheumatoid arthritis.